pedicle marrow signal hyperintensity on short tau ... · 11/08/2011 · table 2: summary of...

ORIGINALRESEARCH

Pedicle Marrow Signal Hyperintensity on ShortTau Inversion Recovery- and T2-WeightedImages: Prevalence and Relationship to ClinicalSymptoms

B. BorgM.T. Modic

N. ObuchowskiG. Cheah

BACKGROUND AND PURPOSE: Lumbar pedicle marrow hyperintense signal on T2- and STIR-weightedimages is not an uncommon finding. We hypothesize that these marrow signal intensity changes andtheir behavior within the pedicle are associated with clinical symptoms and that their improvement orresolution correlates with clinical improvement. We investigated the prevalence of these pediclemarrow changes, associated morphologic abnormalities, and the relationship to symptoms over time.

MATERIALS AND METHODS: Prevalence was evaluated prospectively in 246 patients and retrospec-tively in 400 patients. To analyze the relationship between changes in signal intensity over time andsymptoms, a third group of 30 patients was followed clinically for assessment of pain and functionallimitation and with MR studies for 18 months or until signal intensity changes resolved.

RESULTS: The prevalence of pedicle marrow hyperintensity on T2 and STIR-weighted sequences was1.7%. Associated morphologic abnormalities were pars interarticularis and pedicle fractures anddegenerative facets. In the longitudinal study, pedicle marrow signal hyperintensity on T2- andSTIR-weighted images resolved in 17 patients and persisted in 5 patients. The extent, intensity, andresolution of signal intensity changes significantly related to the degree of functional limitation (P �.01).

CONCLUSIONS: Resolution of pedicle marrow hyperintensity on T2 and STIR-weighted images wasassociated with improved functional testing and a trend toward decreased pain.

ABBREVIATIONS: CI � confidence interval; DFC � degenerative facet change; Pars � pars inter-articularis fracture; Ped � pedicle fracture; STIR � short tau inversion recovery

Changes in MR signal intensity within the pedicles of thelumbar vertebrae are not uncommon and have been re-

ported in association with spondylolysis and degenerativefacet changes.1-5 In these reports, the signal intensity changeswere categorized in a manner similar to vertebral body end-plate marrow changes associated with degenerative disk dis-ease that were described by Modic.6 Although these changes inthe MR signal intensity take 3 main forms (types 1–3), of pri-mary interest here are the type 1 pedicle marrow signal inten-sity changes. Typically, type 1 changes are defined as decreasedsignal intensity on T1 imaging and increased signal intensityon T2/STIR sequences. Type 2 marrow changes are defined asincreased signal intensity on T1 images and more subtle in-creased signal intensity on T2. Type 1 pedicle marrow signalintensity changes are more strongly associated with low backpain and less stable lesions than types 2 and 3.7 For purposes ofbrevity, we henceforth refer to pedicle marrow signal hyperin-tensity on T2 and STIR-weighted images as type 1 pedicle mar-row signal intensity changes.

These type 1 pedicle marrow signal intensity changes andtheir resolution in some patients suggest a healing or stabiliz-ing process; so, understanding their behavior and clinical cor-relates may have implications for the prognosis and manage-

ment of the underlying etiology. Thus, we investigated theprevalence of type 1 pedicle marrow signal intensity changes,identified the associated morphologic abnormalities, and ex-amined the behavior of the changes and how they were relatedto patient symptoms over time. We hypothesized that thesetype 1 pedicle marrow signal intensity changes and their be-havior within the pedicle are associated with clinical symp-toms and may be similar to and behave like type 1 pediclemarrow signal intensity changes in the vertebral body.

Materials and MethodsThis study received approval from our institutional review board and

complied with Health Insurance Portability and Accountability Act

regulations. All patients whose data were collected prospectively pro-

vided signed informed consent.

Prevalence of Type 1 Pedicle Marrow Signal IntensityChangesWe studied 2 distinct populations, 1 prospective population and 1

retrospective population. The prospective group consisted of 246 pa-

tients with acute low back pain, radiculopathy, or both, who pre-

sented within 3 weeks of pain onset and were recruited for an ongoing

prospective study.8 The patients were imaged on 1.5T MR scanners

(Symphony; Siemens, Erlangen, Germany). T1 sagittal images (TR/

TE: 500/12; matrix 192 � 256; 3 averages; sequence time 4 minutes, 20

seconds); T1 axial images (TR/TE: 600/12; matrix 192 � 256; 3 aver-

ages; sequence time 4 minutes, 40 seconds); and T2 sagittal and axial

fast spin-echo images (TR/TE: 5000/120; matrix 192 � 256; 3 aver-

ages; sequence time 4 minutes, 42 seconds.

Received September 14, 2010; accepted after revision January 25, 2011.

From the Imaging (B.B., G.C.) and Neurological (M.T.M.) Institutes, and Quantitative HealthSciences (N.O.), Cleveland Clinic, Cleveland, Ohio.

Please address correspondence to Michael T. Modic, MD, FACR, Cleveland Clinic, 9500Euclid Ave, Cleveland OH 44195; e-mail: [email protected]

http://dx.doi.org/10.3174/ajnr.A2588

SPINE

ORIGINAL

RESEARCH

AJNR Am J Neuroradiol ●:● � ● 2011 � www.ajnr.org 1

Published August 11, 2011 as 10.3174/ajnr.A2588

Copyright 2011 by American Society of Neuroradiology.

The second group was retrospectively identified from patient rec-

ords. Records were selected if the patient had undergone MR imaging

for low back pain at our institution and had neither trauma nor ma-

lignancy as the primary clinical concern or as a finding on the exam-

ination. The last 50 male and 50 female patients with MR imaging for

low back pain from January 1, 2004, to December 31, 2004, were

identified in each of 4 age ranges—�30, 30 – 49, 50 –59, and �60

years of age—for 400 patients in total. All patients were imaged on

1.5T MR scanner systems (Siemens). In addition to the above-men-

tioned protocol, each patient received STIR sagittal imaging (TR/TE:

4200/60; matrix 192 � 256; 3 averages; sequence time 4 minutes, 38

seconds). Images were reviewed by 2 neuroradiologists for consensus

interpretation regarding the presence of type 1 pedicle marrow signal

intensity changes. The diagnoses underlying these changes were re-

corded for both groups.

Presumed Etiology and Longitudinal Changes in Type 1Signal IntensityTo investigate changes in signal intensity over time and their relation-

ship to symptoms, we identified a third group of patients with type 1

pedicle marrow signal intensity changes during routine clinical eval-

uation for low back pain from December 2004 to March 2007. These

patients were entered into a data base to catalog morphologic abnor-

malities associated with the marrow changes. We then recruited pa-

tients from this data base. To be included, patient care must have been

documented in our institution’s electronic health record (Epic Care;

Epic Systems, Verona, Wisconsin) and had sufficient clinical docu-

mentation (including Roland and Likert pain severity scale scores

obtained by phone interview within 1 week of the imaging follow-up)

to determine the clinical course and had at least 1 follow-up MR

examination at our institution. Patients were followed for at least 18

months or until pedicle marrow signal intensity changes resolved,

whichever occurred first; the 18-month stopping point was arbitrarily

chosen. For all patients in the data base, images were reviewed by 2

neuroradiologists for concordant interpretations of the presence or

absence of type 1 pedicle marrow signal intensity and distribution of

signal intensity changes. All images also were reviewed for changes in

MR signal intensity over time, and this change was quantified. Read-

ers were blinded to patient identity and clinical data. Ancillary mor-

phologic findings also were recorded.

To provide semiquantification for purposes of assessing longitu-

dinal change, type 1 pedicle marrow signal intensity change was quan-

tified as follows: the signal hyperintensity was graded by dividing the

pedicle, facets, and pars interarticularis into 7 zones (roughly, 4 quad-

rants of the pedicle on a sagittal STIR image, plus the superior facets,

inferior facets, and pars interarticularis) and summing the zones of

involvement. The marrow edema signal intensity was quantified by

placing a circular region of interest on the area of maximal pedicle

hyperintensity and then determining the intensity score according to

a 4-point linear scale defined by the intensity of normal vertebral body

marrow (0, lowest intensity) and CSF (3, highest intensity) on that

axis.

Statistical AnalysisFor the prevalence of type 1 pedicle marrow signal intensity changes,

95% CIs were constructed for both patient populations, by using the

normal distribution approximation. Fisher exact test was used to test

the association between the presence of type 1 pedicle marrow signal

intensity changes and patient characteristics.

For the longitudinal study, Wilcoxon 2-sample tests were used to

test whether patient age, baseline pain, and baseline signal intensity

scores differed between patients with signal intensity resolution and

those without resolution within 18 months. Kendall tau correlation

coefficients were used to assess the correlation between patient out-

comes (pain score, Roland score, and change in pain score from base-

line) and pedicle marrow signal intensity (intensity, distribution, and

change from baseline in intensity and distribution). Significance was

set at .05. Because these investigations were exploratory, no power

calculations were performed.

Results

Prevalence of Type 1 Pedicle ChangesIn the prospective group, the prevalence of type 1 pedicle mar-row signal intensity change was 1.6% (4/246; 95% CI, 0.0%–3.2%). These patients were female (P � .14), with a mean ageof 54 years (range, 48 – 60 years). Three patients had low backpain, and the fourth had radicular symptoms. In each case, themarrow changes were associated with advanced degenerativechanges in the adjacent facet joints.

In the retrospective group (with STIR sequence), the prev-alence was 1.8% (7/400; 95% CI, 0.0%–3.0%). Two patientswere younger than 30 years, both male. No additional abnor-malities were seen. One patient was in the 30 – 49 year agegroup and 1 patient was in the 50 –59 year group; both patientswere female, with moderate or advanced degenerative changesin adjacent facet joints. Three patients (2 male, 1 female) werein the �60 age group, all with moderate or advanced degen-erative changes in adjacent facet joints.

Type 1 pedicle marrow signal intensity changes were notsignificantly associated with either age or sex in the retrospec-tive group. The conspicuity of the signal intensity changes wasgreater on STIR than T2-weighted sequences but a direct com-parative accuracy between the 2 sequences was not performed.

Etiology and Longitudinal ChangesAt the time of this study, our data base contained records for91 patients. Age distribution and diagnoses are listed in Table1. Thirty patients met the inclusion criteria for longitudinalinvestigation.

Of the 30 patients analyzed longitudinally, the average du-ration of follow-up for all patients was 12 months (range, 4 –22months). Eight did not complete the study because they werelost to or declined additional follow-up. The remaining 22patients were followed for at least 18 months or until the mar-row changes resolved, whichever occurred first. The type 1pedicle marrow signal intensity resolved in 17 patients (meanage, 39 years; mean time to resolution, 11 months; range, 4 –22

Table 1: Structural abnormality compared by age for 91 data basepatients with low back pain and type 1 pedicle marrow changes

Age �30yr

Age 30–50yr Age �50 yr

No. with type 1 changes 27 17 47Sex (M/F) 24/3 3/14 16/31DiagnosisFracture, pars 17 1 5Fracture, pedicles 5 1 1Degenerative facet disease 0 15 41No definitive diagnosis 5

2 Borg � AJNR ● � ● 2011 � www.ajnr.org

months) and persisted in 5 patients. Table 2 summarizes theclinical course and signal intensity changes in the 30 patients.

There were no statistically significant differences in age,baseline pain score (8.0 versus 5.8), baseline signal intensity(4.3 versus 5.0), or baseline signal intensity distribution (8.6versus 9.6) for patients whose pedicle marrow signal intensityresolved compared with patients whose pedicle marrow signalintensity did not resolve.

Roland function score modestly correlated with signal in-tensity (r � 0.28, P � .01), signal intensity distribution (r �0.25, P � .02), and change in distribution since baseline (r �0.29, P � .01). Higher intensity and distribution scores wereassociated with higher (worse) Roland scores, and greater re-ductions in distribution scores from baseline were associatedwith lower (better) Roland scores. The mean pain score in-creased slightly in association with higher pedicle marrow in-tensity and distribution scores. In contrast, the mean Rolandscore increased markedly with higher pedicle marrow inten-sity and distribution scores.

The mean pain scores for those with resolution were 8.0 atbaseline and 5.3 at last follow-up. In the 7 patients withoutmeasurable improvement in pain scores, 5 had degenerative

facet changes. Self-reported pain scores tended to improveover time with concordant resolution of marrow signal inten-sity changes, but this was not statistically significant.

Of the 5 patients without signal intensity resolution by 18months, 3 had an improvement in the distribution and signalintensity and 2 remained unchanged. The mean pain scoreswere 5.8 at baseline and 4.2 at 18 months.

The 8 patients who were lost to follow-up were followed foran average of 9 months. At last follow-up examination, thesignal intensity had improved in 4, remained the same in 3,and worsened in 1. None had complete resolution of the type1 pedicle marrow signal intensity changes. The mean painscores were 7.0 at baseline and 3.9 at last follow-up. In 5 of the8 patients, the pain score had improved at the last follow-upstudy.

In 6 of the 17 patients with resolution, subsequent conver-sion to type 2 marrow changes was seen on the follow-upstudies (Table 2).

In addition to pedicle signal intensity change, 9 of 30 pa-tients had increased signal intensity in the soft tissues adjacentto the facet joints and posterior lateral elements, on STIR-weighted sequences. Four patients had spondylolysis, 3 had

Table 2: Summary of pedicle marrow signal changes, clinical course, posterior paraspinal soft tissue changes, and type 1 to type 2 marrowchanges in 30 patients

Patient No.Patient Age

(yr) DiagnosisSignal

Changes SymptomsaFollow-UpDuration

Soft TissueChangesb

Marrow ConversionType 1 to 2b

17 Patients: signal resolution1 55 DFC Revolved 03 14 Pars Revolved � X X6 64 Ped Revolved �7 16 Pars Revolved � X X9 55 DFC Revolved 0 X13 65 DFC Revolved �15 16 Ped Revolved � X16 62 DFC Revolved 018 11 DFC Revolved �19 20 Pars Revolved � X20 62 DFC Revolved 021 14 Pars Revolved �22 70 DFC Revolved �24 18 Pars Revolved 0 X X25 17 Ped Revolved 0 X27 23 Ped Revolved �29 59 DFC Revolved 0

5 Patients: no signal resolutionfollowed for �18 mo

4 49 DFC Improved � 2111 16 Pars 0 � 18 X14 56 DFC 0 � 18 X23 73 DFC Improved 0 1830 13 Pars Improved � 18 X

8 Patients: no signal resolutionfollowed �18 mo

2 50 Pars 0 �5 18 Pars Improved � X8 66 DFC Improved �10 56 DFC Worse �12 54 Pars Improved �17 42 DFC 0 � X26 50 DFC 0 028 15 Pars Improved �

a 0, no change; �, clinical symptoms improved; �, clinical symptoms worsened.b X, present.


degenerative facet changes, and 2 had a pedicle fracture. Thesoft tissue changes resolved within the follow-up period in all9 patients. In 6 of 9 patients, symptoms improved or resolved.

DiscussionWe found type 1 pedicle marrow signal intensity changes in1.7% of patients who underwent MR of the lumbar spine forback pain. These were most commonly associated with 3 dis-tinct structural abnormalities: degenerative facet disease (Fig1) and fractures of the pars interarticularis (Fig 2) or pedicle(Figs 3 and 4). Although pars and pedicle fractures were morecommon in younger patients and degenerative facet diseasemore so in older patients, neither were exclusive to a single agegroup. Although much less common and not addressed in thisstudy, similar hyperintense pedicle marrow signal intensity onT2- and STIR-weighted images may be associated with infec-tion, hemangioma, osteoid osteoma, or other bony neo-plasms. We determined that both the extent and intensity ofthese marrow changes significantly related to the degree offunctional limitation that was due to low back pain. Self-re-ported pain scores tended to improve over time and with con-cordant resolution of marrow signal intensity changes, butthis was not statistically significant.

Type 1 pedicle marrow signal intensity changes have beenbest characterized in the pediatric patient with low back painassociated with fractures of the pars interarticularis.

Studying pedicle signal intensity changes on MR in pediat-ric patients (n � 37), Sairyo9 concluded that type 1 pediclemarrow signal intensity changes may reflect active stresschanges in the underlying bone, a hypothesis others have pro-

posed.1-3 There is a large amount of literature on a similarmarrow signal intensity pattern in joints outside the spinewhere symptoms and abnormal marrow signal intensity inlong bones correlate with clinical symptoms and trauma orresponse to stress.10-14

Likewise, the association of type 1 pedicle marrow signalintensity changes with pars and pedicle fractures and degen-erative facet changes suggests they are related to biomechani-cal stress created by abnormal spinal segment motion. This ora similar mechanism may be at play in the vertebral bodiesadjacent to degenerated disks. Type 1 vertebral body marrowchanges are associated with degenerative disk disease andmore fluid and variable than type 2.6,7,15-17 Type 1 pediclemarrow signal intensity changes seem to be associated with ahigher prevalence of active low back symptoms15,16,18-20 thantypes 2 and 3 and have a reported prevalence of 4%–15% inpatients with low back pain. Type 1 endplate marrow changesalso have been noted to develop in 8% of patients after diske-ctomy21 and in 40% of patients after chemonucleolysis,22 bothof which may be viewed as models of accelerated disk degen-eration associated with altered biomechanical stress, be itloading, motion, or a combination. That these changes mayreflect altered biomechanical stress is further supported by theobservation that type 1 changes can convert to type 2 or a morenormal-appearing marrow and that conversion is acceleratedand possibly facilitated by fusion and instrumented stabiliza-tion.17,23-26 Six of our 16 patients with signal intensity resolu-tion underwent conversion to a type 2 marrow change (Fig 5).

When stressed, bone behaves according to the Wolfflaw.27 When bone is consistently stressed, it may develop

Fig 1. Type 1 pedicle marrow signal intensity changes associated with degenerative facet disease. A 60-year-old patient with back pain and degenerative facet changes. Parasagittal T1,T2, and STIR images are shown, left to right. On the T1 image, hypointensity is present within the pedicle and superior articular facet of L3 (long arrows). Hyperintensity is noted withinthis same region on T2- and STIR-weighted sequences (long arrows) as well as within the pedicle of L2. Note the subtle hyperintensity within the soft tissues adjacent to the facet jointsat both levels on the STIR image (block arrows).


microfractures followed by osteoblastic repair activity.These microfractures demonstrate abnormal radionuclideuptake during scintigraphy. MR signal intensity changesmay reflect biomechanical stresses that result in remodeledtrabecular bone with microfractures and associated mar-row changes.13,28,29 Others have postulated that a contin-uum in the physiologic response to stress fractures repre-sents an imbalance or uncoupling between bone resorptionand bone formation.30-32 Subsequent complete fracturesare probably a result of exceeding trabecular and corticallimits to withstand the forces applied.

In pedicle fractures, stress changes communicated throughthe pedicle probably produce the signal hyperintensity onSTIR and the fracture itself. In the case of pars interarticularis

fractures, the pedicle changes are probably the result of alteredbiomechanical stress that manifests in the pedicle due to al-tered spinal segment forces secondary to the pars fracture.Likewise, pedicle changes in degenerative facet disease areprobably secondary stress changes. Concomitant CT and MRexaminations were not part of this study, but in the 2 patientswho did have CT and MR, signal intensity changes precededthe development of obvious bony fractures (Fig 3). Althoughspeculative, it may be that the resolution of the marrowchanges and improved functional and pain levels are associ-ated with healing, either bony or fibrous, and reduced biome-chanical stress. We do not know whether or why the changesmight resolve in patients without demonstrable fractures, butwe hypothesize that the resolution might be related to remod-

Fig 2. Type 1 pedicle marrow signal intensity changes associated with an early to progressive pars fracture and absence of signal intensity changes in a terminal spondylolysis in an18-year-old man with back pain and bilateral spondylolysis. Right (A) and left (B) parasagittal MR images of the lumbar spine. In each figure, the T1, T2, STIR, and multiplanar reformattedoblique and parasagittal CT images are shown, from left to right. A, Hypointensity of the L4 right pedicle is evident on T1 with increased signal intensity on T2- and STIR-weighted images(arrows). A relatively acute fracture is noted through the pars interarticularis on the CT images (arrow). B, Signal intensity of the left pedicle is normal on all sequences. The CT imagesreveal an older pars fracture (arrows).


Fig 3. Type 1 pedicle marrow signal intensity changes associated with evolving pedicle fractures in a 13-year-old male adolescent. A, Left type 1 pedicle marrow signal intensity changes,which are best appreciated on the STIR sequence. From top to bottom, each row shows T1-, T2-, and STIR-weighted sequences. The MR study on February 9, 2005, demonstrates increasedsignal intensity within the left pedicle and proximal superior facet, which is best appreciated on the STIR sequence (arrow). He was treated conservatively and the back pain improved.The follow-up study on March 23, 2005, demonstrates some improvement in the hyperintensity of the left L5 pedicle. A follow-up MR study on August 4, 2005, demonstrates increasedtype 1 pedicle marrow changes of L5 bilaterally with a fracture line at the junction of the pedicle and superior articular facets (arrow). A follow-up study from February 20, 2006, showssome improvement of the increased signal intensity on STIR and T2 (arrows), and the previous fracture line is no longer appreciated. Similar changes were seen on the right. The patient’sback pain was less severe but still present. B, Axial T2 MR images (top row) through the L5 pedicle on February 9, 2005, and August 4, 2005, and axial CT images (bottom row) throughthe L5 pedicle on February 18, 2005, and August 8, 2005. The CT obtained on February 18, 2005, was read as negative for fracture. The follow-up MR image demonstrates bilateral fracturelines through the L5 pedicles. The follow-up CT from August 8, 2005, shows clearly demarcated fractures through the junction of the pedicle and superior facet of L5 bilaterally (arrows).


Fig 4. Type 1 pedicle marrow signal intensity changes associated with new and old pedicle fractures in a 64-year-old woman. A, Right parasagittal T1-, T2-, and STIR-weighted imagesthat demonstrate a discrete fracture line through the pedicles of L4 bilaterally without pedicle marrow signal intensity changes (long arrow) and a less obvious fracture line on T1 imagesthrough the L5 pedicle with concomitant type 1 pedicle marrow changes (short arrows). Signal intensity changes at L5 and clinical symptoms had resolved at 8 months of follow-up. B,Right and left parasagittal multiplanar reformatted CT images through the lumbar spine and axial images through the pedicles of L5. Note the lucent appearance of the subacute fracturesite through the pedicles on the parasagittal multiplanar reformatted images and adjacent axial CTs and the less well-defined fracture and adjacent marrow signal intensity alterationthrough the pedicles on the axial MR images (arrows).The signal intensity change is more obvious on the axial MR image on the right. Note the sclerotic appearance of an older fracturesite through the L4 pedicle on the CT images.

Fig 5. A 25-year-old man with back pain. The left parasagittal T1, T2, and STIR images (left to right) from August 3, 2006, and January 19, 2007, which demonstrate type 1 pedicle marrowchanges on the August 3, 2006, study. The hyperintensity on T2 and STIR images has resolved by the second study. On the T1 images, the decreased marrow signal intensity (type I) notedinitially (August 3, 2006) has converted to a type 2 marrow (increased signal intensity on T1) on the second study (January 19, 2007).


eled bone that has greater stability or healed microfractures.The resolution of changes in patients who have degenerativefacets remains the most perplexing issue because this is achronic process, unless some degree of unidentified stabiliza-tion does occur.

Posterior paraspinal soft tissue hyperintensity that is moreconspicuous on STIR sequences has been reported in associa-tion with degenerative spinal changes.33,34 Adjacent soft tissuehyperintensity on STIR sequences in almost a third of ourpatients suggests that in the symptomatic stage, altered biome-chanical forces affect not just the bone but exert secondaryeffects within the adjacent soft tissues as well. We saw these softtissue changes in patients with pars and pedicle fractures as well asdegenerative facet disease. Their resolution along with the mar-row hyperintensity on STIR would support an acute stage thatalters biomechanics and is then followed by subsequent stabiliza-tion and adaptation over time (Figs 1 and 6).

Further questions are whether these changes indicate ahigher risk for fracture and whether different therapies canalter the clinical course, by using marrow changes as a marker.In a study by Sakai et al35 of 17 adolescent patients with freshspondylolysis, signal intensity changes resolved by 3 months inmost patients but persisted longer in patients who did notcomply with conservative treatment. Our observations wouldbenefit from further, systematic evaluation in a larger patientpopulation with more rigorous follow-up and concordant CTexaminations, which could provide important informationrelative to boney trabecular and cortical changes. Finally, sucha study should control for different types of clinical interven-

tion versus symptom and pedicle marrow signal intensity res-olution that was not done in this study.

ConclusionsOur results suggest that type 1 pedicle marrow signal intensityis a marker for a spectrum of bony changes (eg, remodeling,stress fracture, and complete fracture) most commonly asso-ciated with 3 distinct structural abnormalities (pedicle frac-tures, pars fractures, and degenerative facets) and clinicallyobservable pain and functional limitation. The resolution ofthese changes is associated with improved functional testingand a trend toward decreased pain. If a component of thisprocess is altered biomechanical force, recognizing thesechanges at an early stage may permit modification of therapyfor a subset of symptomatic patients with type 1 pedicle mar-row signal intensity changes. Furthermore, in adolescents,where the question of a pars or pedicle fracture is often animportant differential consideration in the patient with backpain, MR imaging should play a more routine role in the eval-uation. Type 1 pedicle marrow signal intensity changes may beimportant in identifying a subgroup that is at risk for fractureor who may benefit from more conservative measures to re-duce biomechanical stress.

AppendixThe Likert scale is an ordered, 1D dimensional scale fromwhich respondents choose 1 option that best aligns with theirview. There are typically between 4 and 7 options with 5 beingthe most common. For example, the 5-point traditional Likert

Fig 6. Type 1 pedicle marrow signal intensity changes and associated soft tissue hyperintensity on T2- and STIR-weighted sequences associated with pars fractures of L2 in a 14-year-oldfemale adolescent. Right parasagittal T1, T2, and STIR images from May 18, 2006, and November 21, 2006. On the initial study, type 1 pedicle marrow signal intensity changes are notedwithin the L2 pedicle and superior articular facet (long arrow). The signal intensity also is increased within the soft tissue adjacent to the L2 superior facet (short arrow) on the STIR-weightedsequences. On the follow-up study, the marrow changes have converted from type 1 to type 2 (long arrow), and the soft tissue changes have resolved (short arrow). The patient was improvedclinically.


scale includes the following choices: 1) strongly agree, 2) tendto agree, 3) neither agree or disagree, 4) tend to disagree, and5) strongly disagree. By dropping number 3 (neither agree ordisagree), the 4-point Likert scale becomes a forced choice.37

The Roland-Morris disability questionnaire is a widelyused health status measure for low back pain. References re-garding this scale are included.


DISCLOSURES: Nancy Obuchowski, Research Support (including provision of equipment ormaterials): Siemens Medical, Inc.; iCAD; Details: I am a biostatistician. My departmentcontracts with Siemens and iCAD for data analysis. I perform some of the data analysis,but I personally receive nothing from Siemens or iCAD.

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